Cause-effect relation between hyperfibrinogenemia and vascular disease. Blood 2004 Mar 01;103(5):1728-34
Date
11/15/2003Pubmed ID
14615369DOI
10.1182/blood-2003-08-2886Scopus ID
2-s2.0-10744231546 (requires institutional sign-in at Scopus site) 85 CitationsAbstract
Elevated plasma levels of fibrinogen are associated with the presence of cardiovascular disease, but it is controversial whether elevated fibrinogen causally imparts an increased risk, and as such is a true modifier of cardiovascular disease, or is merely associated with disease. By investigating a transgenic mouse model of hyperfibrinogenemia, we show that elevated plasma fibrinogen concentration (1) elicits augmented fibrin deposition in specific organs, (2) interacts with an independent modifier of hemostatic activity to regulate fibrin turnover/deposition, (3) exacerbates neointimal hyperplasia in an experimental model of stasis-induced vascular remodeling, yet (4) may suppress thrombin generation in response to a procoagulant challenge. These findings provide direct experimental evidence that hyperfibrinogenemia is more than a by-product of cardiovascular disease and may function independently or interactively to modulate the severity and/or progression of vascular disease.
Author List
Kerlin B, Cooley BC, Isermann BH, Hernandez I, Sood R, Zogg M, Hendrickson SB, Mosesson MW, Lord S, Weiler HAuthor
Rashmi Sood PhD Associate Professor in the Pathology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCarotid Arteries
Chlorides
Cross-Linking Reagents
Dimerization
Disease Models, Animal
Enzyme-Linked Immunosorbent Assay
Ferric Compounds
Fibrinogen
Mice
Mice, Transgenic
Protein Binding
Thrombin
Thrombosis
Vascular Diseases
